Histopathological characterization and shedding dynamics of guineafowl (Numida meleagris) intravenously infected with a H6N2 low pathogenicity avian influenza virus

Authors: DIMITROV, KIRIL - National Diagnostic And Research Veterinary Medicine Institute; ZARKOV, IVAN - Trakia University; DINEV, IVAN - Trakia University; GOUJGOULOVA, GABRIELA - National Diagnostic And Research Veterinary Medicine Institute; Miller, Patti; Suarez, David

Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/2/2016
Publication Date: 2/2/2016
Citation: Dimitrov, K.M., Zarkov, I.S., Dinev, I., Goujgoulova, G.V., Miller, P.J., Suarez, D.L. 2016. Histopathological characterization and shedding dynamics of guineafowl (Numida meleagris) intravenously infected with a H6N2 low pathogenicity avian influenza virus. Avian Diseases. 60(1s):279-85. https://doi.org/10.1637/11141-050815-Reg.
DOI: https://doi.org/10.1637/11141-050815-Reg

Interpretive Summary: Guineafowl of different ages were inoculated intravenously with a H6N2 wild waterfowl–origin low pathogenicity avian influenza virus (LPAIV). No clinical disease was observed. The infected birds had atrophy of the spleen, thymus, and cloacal bursa when compared with the noninfected control groups. The central and peripheral lymphoid tissues presented either lymphoproliferative or degenerative lesions that increased in intensity from 14 to 21 days postinoculation (DPI). Lymphoid depletion was present in the bursa, thymic lobes, and spleen T-dependent zone. In contrast, lymphoid proliferation was observed in liver, pancreas, and spleen B-dependent zone. Bronchus associated lymphoid tissue hyperplasia was observed in the lungs of the birds at 14 and 21 DPI. The virus was detected by virus isolation and reverse transcription PCR from both oropharyngeal and cloacal swabs with higher isolation rates from the latter. Most birds from the LPAIV inoculated groups shed virus up to 7 DPI. The virus was infrequently isolated from lung, kidney, liver, bursa, or spleen of infected birds until 14 DPI and from two samples (kidney and spleen, 1-yr-old birds) at 21 DPI. These data indicate that the wild bird–origin LPAIV used in this study caused pantropic infection in guineafowl when inoculated intravenously.

Technical Abstract: Guineafowl of different ages were inoculated intravenously with an H6N2 wild waterfowl-origin low-pathogenicity type A avian influenza virus (LPAI). No evidence of clinical disease was observed. The examined infected birds had atrophy of the spleen, thymus, and cloacal bursa when compared to the non-infected control groups. The central and peripheral lymphoid tissues presented either lymphoproliferative or degenerative lesions that increased in intensity from 14 to 21 days postinoculation (DPI). Lymphoid depletion was present in the bursa, thymic lobules, and T-dependent zone of the spleen’s Malpighi bodies. In contrast, lymphoid proliferation was observed in the cecal tonsils, liver, lungs, and B-dependent zone of the spleen. Interstitial pneumonia was observed in the lungs of the birds at 14 and 21 DPI. The virus was recovered by virus isolation (VI) from both oropharyngeal and cloacal swabs with higher isolation rate from the latter. The birds from all of the experimental groups were shedding viruses from 3 to 10 DPI, with the highest rate at 7 DPI. Two birds from the two-month-old group were shedding viruses for as long as 14 DPI. Virus recovery was successful from different organs until 14 DPI, and also from two samples (kidney and spleen, one-year-old birds) at 21 DPI. Real-time reverse-transcriptase polymerase chain reaction was performed to detect viral RNA of avian influenza virus, and the obtained results supported VI findings. These data indicate that the low-pathogenicity wild bird-origin influenza virus used in this study was pantropic during intravenous route of infection in guineafowl.